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. 2017 Feb 28;108(2):256–266. doi: 10.1111/cas.13126

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© 2016 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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Key genes and pathways in oral squamous cell carcinoma. Somatic mutations and copy number alterations indicated mutual exclusivity for receptor tyrosine kinases (RTKs), CDKN2A, and PIK3CA. CDKN2A deletions were exclusive with TP53 somatic mutations, whereas PIK3CA amplifications were cooperative with TP53 somatic mutations. The number of patients with RTK amplification and distant metastasis was nine. Meanwhile, 24 (37 patients) and 43% (21 patients) had RTK amplification and distant metastasis, respectively. The right panel of the figure shows approved molecular‐targeted drugs against RTKs in malignant tumors. In head and neck squamous cell carcinoma (HNSCC), the only approved drug is cetuximab.